Cited by 1,076Gut microbiota and healthMicrobial Metabolites in Food BiotechnologyProbiotics and Fermented Foods

Responses of Gut Microbiota and Glucose and Lipid Metabolism to Prebiotics in Genetic Obese and Diet-Induced Leptin-Resistant Mice

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Everard, Amandine, Lazarevic, Vladimir, Derrien, Muriel, Girard, Myriam, Muccioli, Giulio G., Neyrinck, Audrey M., Possemiers, Sam, Van Holle, Ann +5 more·2011·Diabetes

Abstract

OBJECTIVE: To investigate deep and comprehensive analysis of gut microbial communities and biological parameters after prebiotic administration in obese and diabetic mice. RESEARCH DESIGN AND METHODS: Genetic (ob/ob) or diet-induced obese and diabetic mice were chronically fed with prebiotic-enriched diet or with a control diet. Extensive gut microbiota analyses, including quantitative PCR, pyrosequencing of the 16S rRNA, and phylogenetic microarrays, were performed in ob/ob mice. The impact of gut microbiota modulation on leptin sensitivity was investigated in diet-induced leptin-resistant mice. Metabolic parameters, gene expression, glucose homeostasis, and enteroendocrine-related L-cell function were documented in both models. RESULTS: In ob/ob mice, prebiotic feeding decreased Firmicutes and increased Bacteroidetes phyla, but also changed 102 distinct taxa, 16 of which displayed a >10-fold change in abundance. In addition, prebiotics improved glucose tolerance, increased L-cell number and associated parameters (intestinal proglucagon mRNA expression and plasma glucagon-like peptide-1 levels), and reduced fat-mass development, oxidative stress, and low-grade inflammation. In high fat–fed mice, prebiotic treatment improved leptin sensitivity as well as metabolic parameters. CONCLUSIONS: We conclude that specific gut microbiota modulation improves glucose homeostasis, leptin sensitivity, and target enteroendocrine cell activity in obese and diabetic mice. By profiling the gut microbiota, we identified a catalog of putative bacterial targets that may affect host metabolism in obesity and diabetes.

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  • Some prebiotics, including the polysaccharide inulin as well as FOS and GOS, increase production of both GLP-1 and PYY.

    “Some prebiotics, a polysaccharide inulin as well as FOS and GOS were shown to increase the production of both GLP-1 and PYY (Cani et al., 2005;Everard et al., 2011).”

    From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Everard et al., 2011

    The Methods (Mice; page unavailable) identify oligofructose as the prebiotic given to the mice, and the Results (L-cell number in obese mice; page unavailable) report increased portal plasma GLP-1 after treatment. The paper does not report increased PYY or test inulin and GOS as separate treatments, so it does not support the claim that all three increase both peptides. (LLM, conf=0.90)

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Authors
Everard, A., Lazarevic, V., Derrien, M., Girard, M., Muccioli, G. G., Neyrinck, A. M., Possemiers, S., Van Holle, A., François, P., de Vos, W. M., Delzenne, N. M., Schrenzel, J., & Cani, P. D.
Affiliations
  • UCLouvain (BE)
  • Genomic Research Laboratory, Geneva University Hospitals, Geneva, Switzerland
  • TiFN (NL)
  • University Hospital of Geneva (CH)
  • Ghent University (BE)
  • Laboratory of Microbial Ecology and Technology, Ghent University, Ghent, Belgium
  • Laboratory of Microbiology, Wageningen University, Wageningen, the Netherlands
Corresponding author
Cani, Patrice D.
Venue
Diabetes
Published
2011-10-17
Volume
60
Issue
11
Pages
2775-2786
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
OpenAlex
W2153075279
Cited by
1,076
References
8
Citations by year
2026: 26 · 2025: 49 · 2024: 70 · 2023: 59 · 2022: 114 · 2021: 92 · 2020: 88 · 2019: 88 · 2018: 90 · 2017: 85 · 2016: 94 · 2015: 81 · 2014: 55 · 2013: 49 · 2012: 33
FWCI
17.94
Type
journal article
Language
en
Open access
Locations
  • Diabetes (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • Archive ouverte UNIGE (University of Geneva) (publishedVersion)
  • Socio-Environmental Systems Modeling (acceptedVersion)
  • Digital Access to Libraries (submittedVersion)
  • Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
Funders
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (124717)
  • Société Francophone du Diabète
  • Fonds Spéciaux de Recherche
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Health Sciences › Nursing › Nutrition and Dietetics › Microbial Metabolites in Food Biotechnology
  • Life Sciences › Agricultural and Biological Sciences › Food Science › Probiotics and Fermented Foods
Keywords
prebiotics, gut microbiota, obesity, leptin resistance, glucose metabolism, lipid metabolism, glucose tolerance, enteroendocrine cells, L cells, glucagon-like peptide-1, proglucagon, Firmicutes, Bacteroidetes, oxidative stress, low-grade inflammation, fat mass, ob/ob mice, high-fat diet
MeSH terms
Animals, Cecum, Colon, Diabetes Mellitus, Type 2, Dietary Fats, Gene Expression Regulation, Gram-Negative Bacteria, Gram-Positive Bacteria, Hyperglycemia, Hyperlipidemias, Mice, Inbred C57BL, Mice, Obese, Obesity, RNA, Messenger, Glucose Intolerance, Enteroendocrine Cells, Leptin, Mice, Glucagon-Like Peptide 1, Proglucagon, Prebiotics, Molecular Typing

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